Abstract

It has been proposed that the cochlear microphonic (CM) is produced by a modulated potassium-current through channels in the apical membrane of the hair cells. In support of this concept, Salt and Konishi [J. Acoust. Soc. Am. 66, S47 (1979)] have found that electrophoretically applied tetraethylammonium (TEA; a blocker of K channels of excitable membranes) reduces the CM while raising the endocochlear potential. However, two lines of evidence suggest that these pathways might not be K-selective: (1) Cory and Hudspeth [Nature (in press)] have shown in an in vitro lower-vertebrate hair cell system that the microprohie-producing ion channels are not K selective, since numerous ions can be accommodated. (2) We have observed that injections into scala media of about 50 nl each of phentolamine (1 mM), serotoxin (5 mM), or EGTA (1 mM) in artificial endolymph produce effects similar to those reported for TEA. Control injections produced no effect. The diversity of the known primary actions of each of these agents (alpha-adrenergic blocker, neurotransmitter, and calcium chelating agent, respectively) suggests that TEA may not be acting on a strictly K-selective channel. [Supported by NSF and NIH.]

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